The early stages of infancy, and in particular, the neonatal period, are periods of rapid cell growth and proliferation. Consequently, oxygen consumption is high compared to that of older children and adults. During these early stages, there is a limitation on the infant's ability to increase stroke volume; thus, cardiac output and oxygen delivery are dependent on heart rate.
In the newborn infant, cerebral blood flow is pressure-passive; as a result, cerebral blood flow tracks perfusion pressures more closely than older patients. In addition, the circulatory system of the developing brain has watershed areas that are particularly vulnerable to ischemia and/or hypoxia. Inadequate oxygen delivery can result in the development of hypoxic/ischemic encephalopathy, the major cause of long-term neurological disorders in children.
With regard to oxygen carrying capacity, the oxyhemoglobin dissociation curve of fetal hemoglobin is shifted to the left; this provides a physiologic advantage to the fetus but may be disadvantageous in post-natal life since oxygen release at the tissue level may be impaired. Neonatal transfusions are often performed in critically ill newborns to increase tissue oxygen delivery by decreasing the P50 (oxygen tension at half saturation of blood) and improving release at the tissue level.
To further complicate the neonatal period, the increase in arterial oxygen partial pressure (PaO2) that occurs following the initiation of air breathing is sufficient to shut down erythropoietin synthesis and release. In the normal term infant, significant red cell production will only resume after “physiologic anemia” develops between 6-12 weeks after birth.
For premature infants, anemia may have more immediate and deleterious significance. In the first few weeks of embryogenesis, fetal erythrocytes are produced in the yolk sac. This site is succeeded by the fetal liver, which, by the end of the first trimester, has become the primary site of erythropoiesis. Bone marrow then begins to take on a more active role in producing erythrocytes. By approximately 32 weeks' gestation, the burden of erythrocyte production in the fetus is shared evenly by the liver and bone marrow. By 40 weeks' gestation, the marrow is the sole erythroid organ. Premature delivery does not accelerate the ontogeny of these processes.
Shortened red blood cell life span or hemolysis also contributes to premature neonatal anemia. The average life span of a neonatal RBC is only one half to two thirds that of the RBC life span in an adult. Cells of the most immature infants may survive only 35-50 days. The shortened RBC life span of the neonate is a result of multiple factors, including diminished levels of intracellular ATP, carnitine, and enzyme activity; increased susceptibility to lipid peroxidation; and increased susceptibility of the cell membrane to fragmentation.
Finally, blood loss may contribute to the development of premature neonatal anemia. If the neonate is held above the placenta for a time after delivery, a fetal-placental transfusion may occur. More commonly, because of the need to closely monitor the tiny infant, frequent samples of blood are removed for various tests. Because the smallest patients may be born with as little as 40 mL of blood in their circulation, withdrawing a significant percentage of an infant's blood volume in a short period is relatively easy. Taken together, the premature infant is at risk for the development of anemia because of limited erythrocyte synthesis, diminished RBC life span, and increased loss of RBCs. With regard to treatment, packed red blood cell (PRBC) transfusions continue to be the mainstay of therapy for premature neonatal anemia.
In addition to anemia, hyperkalemia may also complicate the first few days in very low birth weight infants. Hyperkalemia (serum potassium level>6 mEq/L) usually presents within the first 72 hours of life and is the result of immature distal tubular function and a state of relative hypoaldosteronism with a compromised ability to excrete potassium. It may also be due, in part, to a shift of potassium from the intracellular space to extracellular space associated with a decrease in Na+−K+−ATPase activity. In sick newborn infants with renal dysfunction, hyperkalemia may occur, particularly when combined with metabolic acidosis and a hypercatabolic state. Rarer causes of hyperkalemia include hypoadrenal crises, massive hemolysis, tissue damage or excessive administration of potassium as drugs or intravenous fluids. Doctors often request washed red blood cells for patients with hyperkalemia.